Alginate production in and the associated mucoid phenotype of isolates from cystic fibrosis patients are under the control of the cluster. This group of genes encodes AlgU, the equivalent of the extreme heat shock σ factor σ in Gram-negative bacteria, the AlgU-cognate anti-σ factor MucA, the periplasmic protein MucB and a serine protease homologue, MucD. While or act as negative regulators of AlgU, the function of is not known. In this study the role of in physiology and alginate production has been addressed. Insertional inactivation of in the wild-type strain PAO1 did not cause any overt effects on alginate synthesis. However, it affected growth of under conditions of combined elevated temperature and increased ionic strength or osmolarity. inactivation of in or mutant backgrounds resulted in a mucoid phenotype when the cells were grown under combined stress conditions of elevated temperature and osmolarity. Each of the stress factors tested separately did not cause comparable effects. The combined stress factors were not sufficient to cause phenotypically appreciable enhancement of alginate production in or mutants unless was also inactivated. These findings support a negative regulatory role of in alginate production by indicate additive effects of genes in the regulation of mucoidy in this organism and suggest that multiple stress signals and recognition systems participate in the regulation of -dependent functions.

Keyword(s): anti-sigma , mucoidyle and Sigma factors

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